Faculty Opinions recommendation of rpoS mutations and loss of general stress resistance in Escherichia coli populations as a consequence of conflict between competing stress responses.

Author(s):  
Thomas Nystrom
2002 ◽  
Vol 184 (3) ◽  
pp. 806-811 ◽  
Author(s):  
Lucinda Notley-McRobb ◽  
Thea King ◽  
Thomas Ferenci

ABSTRACT The general stress resistance of Escherichia coli is controlled by the RpoS sigma factor (φS), but mutations in rpoS are surprisingly common in natural and laboratory populations. Evidence for the selective advantage of losing rpoS was obtained from experiments with nutrient-limited bacteria at different growth rates. Wild-type bacteria were rapidly displaced by rpoS mutants in both glucose- and nitrogen-limited chemostat populations. Nutrient limitation led to selection and sweeps of rpoS null mutations and loss of general stress resistance. The rate of takeover by rpoS mutants was most rapid (within 10 generations of culture) in slower-growing populations that initially express higher φS levels. Competition for core RNA polymerase is the likeliest explanation for reduced expression from distinct promoters dependent on φ70 and involved in the hunger response to nutrient limitation. Indeed, the mutation of rpoS led to significantly higher expression of genes contributing to the high-affinity glucose scavenging system required for the hunger response. Hence, rpoS polymorphism in E. coli populations may be viewed as the result of competition between the hunger response, which requires sigma factors other than φS for expression, and the maintenance of the ability to withstand external stresses. The extent of external stress significantly influences the spread of rpoS mutations. When acid stress was simultaneously applied to glucose-limited cultures, both the phenotype and frequency of rpoS mutations were attenuated in line with the level of stress. The conflict between the hunger response and maintenance of stress resistance is a potential weakness in bacterial regulation.


Genetics ◽  
2004 ◽  
Vol 166 (2) ◽  
pp. 669-680 ◽  
Author(s):  
Mary-Jane Lombardo ◽  
Ildiko Aponyi ◽  
Susan M Rosenberg

Abstract Microbial cells under growth-limiting stress can generate mutations by mechanisms distinct from those in rapidly growing cells. These mechanisms might be specific stress responses that increase mutation rates, potentially altering rates of evolution, or might reflect non-stress-specific processes in rare growing cells. In an Escherichia coli model system, both frameshift reversion mutations and gene amplifications occur as apparent starvation-induced mutations. Whereas frameshift reversion (“point mutation”) requires recombination proteins, the SOS response, and error-prone DNA polymerase IV (DinB), amplification requires neither SOS nor pol IV. We report that both point mutation and amplification require the stationary-phase and general stress response transcription factor RpoS (σS). Growth-dependent mutation does not. Alternative interpretations are excluded. The results imply, first, that point mutation and amplification are stress responses that occur in differentiated stationary-phase (not rare growing) cells and, second, that transient genetic instability, producing both point mutation and genome rearrangement, may be a previously unrecognized component of the RpoS-dependent general stress response.


Microbiology ◽  
2014 ◽  
Vol 160 (8) ◽  
pp. 1690-1704 ◽  
Author(s):  
Jasmin Gundlach ◽  
Jeannette Winter

Exposure of cells to stress impairs cellular functions and may cause killing or adaptation. Adaptation can be facilitated by stress-induced mutagenesis or epigenetic changes, i.e. phenotypic variation without mutations. Upon exposure to HOCl, which is produced by the innate immune system upon bacterial infection, bacteria trigger stress responses that enable increased survival against the stress. Here, we addressed the question whether bacteria can adapt to high HOCl doses and if so, how the acquired resistance is facilitated. We evolved Escherichia coli cells for maximum HOCl resistance by successively increasing the HOCl concentration in the cultivation medium. HOCl-resistant cells showed broad stress resistance but did not carry any chromosomal mutations as revealed by whole-genome sequencing. According to proteome analysis and analysis of transcript levels of stress-related genes, HOCl resistance was accompanied by altered levels of outer-membrane proteins A, C, F and W, and, most prominently, a constitutively expressed OxyR regulon. Induction of the OxyR regulon is facilitated by a partially oxidized OxyR leading to increased levels of antioxidant proteins such as Dps, AhpC/AhpF and KatG. These changes were maintained in evolved strains even when they were cultivated without stress for a prolonged time, indicating epigenetic changes contributed to stress resistance. This indicated that maximum HOCl resistance was conferred by the accumulated action of the OxyR stress response and other factors such as altered levels of outer-membrane proteins.


2016 ◽  
Vol 82 (15) ◽  
pp. 4628-4640 ◽  
Author(s):  
Yinka Somorin ◽  
Florence Abram ◽  
Fiona Brennan ◽  
Conor O'Byrne

ABSTRACTAlthoughEscherichia coliis generally considered to be predominantly a commensal of the gastrointestinal tract, a number of recent studies suggest that it is also capable of long-term survival and growth in environments outside the host. As the extraintestinal physical and chemical conditions are often different from those within the host, it is possible that distinct genetic adaptations may be required to enable this transition. Several studies have shown a trade-off between growth and stress resistance in nutrient-poor environments, with lesions in therpoSlocus, which encodes the stress sigma factor RpoS (σS). In this study, we investigated a unique collection of long-term soil-persistentE. coliisolates to determine whether the RpoS-controlled general stress response is altered during adaptation to a nutrient-poor extraintestinal environment. The sequence of therpoSlocus was found to be highly conserved in these isolates, and no nonsense or frameshift mutations were detected. Known RpoS-dependent phenotypes, including glycogen synthesis and γ-aminobutyrate production, were found to be conserved in all strains. All strains expressed the full-length RpoS protein, which was fully functional using the RpoS-dependent promoter reporter fusion PgadX::gfp. RpoS was shown to be essential for long-term soil survival ofE. coli, since mutants lackingrpoSlost viability rapidly in soil survival assays. Thus, despite some phenotypic heterogeneity, the soil-persistent strains all retained a fully functional RpoS-regulated general stress response, which we interpret to indicate that the stresses encountered in soil provide a strong selective pressure for maintaining stress resistance, despite limited nutrient availability.IMPORTANCEEscherichia colihas been, and continues to be, used as an important indicator species reflecting potential fecal contamination events in the environment. However, recent studies have questioned the validity of this, sinceE. colihas been found to be capable of long-term colonization of soils. This study investigated whether long-term soil-persistentE. colistrains have evolved altered stress resistance characteristics. In particular, the study investigated whether the main regulator of genes involved in stress protection, the sigma factor RpoS, has been altered in the soil-persistent strains. The results show that RpoS stress protection is fully conserved in soil-persistent strains ofE. coli. They also show that loss of therpoSgene dramatically reduces the ability of this organism to survive in a soil environment. Overall, the results indicate that soil represents a stressful environment forE. coli, and their survival in it requires that they deploy a full stress protection response.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Lixia Fang ◽  
Jie Fan ◽  
Shulei Luo ◽  
Yaru Chen ◽  
Congya Wang ◽  
...  

AbstractTo construct a superior microbial cell factory for chemical synthesis, a major challenge is to fully exploit cellular potential by identifying and engineering beneficial gene targets in sophisticated metabolic networks. Here, we take advantage of CRISPR interference (CRISPRi) and omics analyses to systematically identify beneficial genes that can be engineered to promote free fatty acids (FFAs) production in Escherichia coli. CRISPRi-mediated genetic perturbation enables the identification of 30 beneficial genes from 108 targets related to FFA metabolism. Then, omics analyses of the FFAs-overproducing strains and a control strain enable the identification of another 26 beneficial genes that are seemingly irrelevant to FFA metabolism. Combinatorial perturbation of four beneficial genes involving cellular stress responses results in a recombinant strain ihfAL−-aidB+-ryfAM−-gadAH−, producing 30.0 g L−1 FFAs in fed-batch fermentation, the maximum titer in E. coli reported to date. Our findings are of help in rewiring cellular metabolism and interwoven intracellular processes to facilitate high-titer production of biochemicals.


2014 ◽  
Vol 196 (8) ◽  
pp. 589-600 ◽  
Author(s):  
Heloisa F. Galbiati ◽  
Natalia P. Taschner ◽  
Beny Spira

2022 ◽  
Vol 8 (1) ◽  
pp. 50
Author(s):  
Yifan Li ◽  
Xiya Meng ◽  
Degang Guo ◽  
Jia Gao ◽  
Qiwei Huang ◽  
...  

Light is perceived by photoreceptors in fungi and further integrated into the stress-activated MAPK HOG pathway, and thereby potentially activates the expression of genes for stress responses. This indicates that the precise control of light conditions can likely improve the conidial yield and stress resistance to guarantee the low cost and long shelf life of Trichoderma-based biocontrol agents and biofertilizers. In this study, effects of wavelengths and intensities of light on conidial yield and stress tolerance to osmotic, oxidative and pH stresses in Trichoderma guizhouense were investigated. We found that 2 μmol photons/(m2 × s) of blue light increased the conidial yield more than 1000 folds as compared to dark condition and simultaneously enhanced conidial stress resistance. The enhanced conidial stress resistance is probably due to the upregulated stress-related genes in blue light, which is under the control of the blue light receptor BLR1 and the MAP kinase HOG1.


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